Inhibition of Dectin-1 Alleviates Neuroinflammatory Injury by Attenuating NLRP3 Inflammasome-Mediated Pyroptosis After Intracerebral Hemorrhage in Mice: Preliminary Study Results

Ding, Zhiquan; Zhong, Zhenzhong; Wang, Jun; Zhang, Run; Shao, Jinlian; Li, Yulong; Wu, Guiwei; Tu, Huiru; Yuan, Wen; Sun, Haitao; Wang, Qinghua

doi:10.2147/jir.s384020

Cited by 13 publications

(3 citation statements)

References 48 publications

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“… [ 82 ] Dectin-1 Dectin-1 blockade inhibits NLRP3 activation. [ 83 ] Sennoside A It inactivates caspase-1 to inhibit NLRP3 and AIM2 inflammasome-involved inflammation. [ 84 ] Total extract of Abelmoschus manihot L Inhibition of caspase-8/caspase-3/NLRP3/GSDME signaling.…”

Section: Factors Affecting Rt-induced Pyroptosismentioning

confidence: 99%

Pyroptotic cell death: an emerging therapeutic opportunity for radiotherapy

Li,

Yang,

Zhang

et al. 2024

Cell Death Discov.

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Pyroptotic cell death, an inflammatory form of programmed cell death (PCD), is emerging as a potential therapeutic opportunity for radiotherapy (RT). RT is commonly used for cancer treatment, but its effectiveness can be limited by tumor resistance and adverse effects on healthy tissues. Pyroptosis, characterized by cell swelling, membrane rupture, and release of pro-inflammatory cytokines, has been shown to enhance the immune response against cancer cells. By inducing pyroptotic cell death in tumor cells, RT has the potential to enhance treatment outcomes by stimulating anti-tumor immune responses and improving the overall efficacy of RT. Furthermore, the release of danger signals from pyroptotic cells can promote the recruitment and activation of immune cells, leading to a systemic immune response that may target distant metastases. Although further research is needed to fully understand the mechanisms and optimize the use of pyroptotic cell death in RT, it holds promise as a novel therapeutic strategy for improving cancer treatment outcomes. This review aims to synthesize recent research on the regulatory mechanisms underlying radiation-induced pyroptosis and to elucidate the potential significance of this process in RT. The insights gained from this analysis may inform strategies to enhance the efficacy of RT for tumors.

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Section: Factors Affecting Rt-induced Pyroptosismentioning

confidence: 99%

Pyroptotic cell death: an emerging therapeutic opportunity for radiotherapy

Li,

Yang,

Zhang

et al. 2024

Cell Death Discov.

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“…Upon inflammatory stimulation, the NLRP3 inflammasome aggregates, resulting in the activation of Caspase-1 . Activated Caspase-1 further cleaves and activates IL-1β and IL-18, inducing neuronal pyroptosis (Ding et al, 2022).…”

Section: Classical Activation Of Microglia Leads To Neuronal Pyroptosismentioning

confidence: 99%

To re-examine the intersection of microglial activation and neuroinflammation in neurodegenerative diseases from the perspective of pyroptosis

Li,

Zhu

2023

Front. Aging Neurosci.

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Neurodegenerative diseases (NDs), such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and motor neuron disease, are diseases characterized by neuronal damage and dysfunction. NDs are considered to be a multifactorial disease with diverse etiologies (immune, inflammatory, aging, genetic, etc.) and complex pathophysiological processes. Previous studies have found that neuroinflammation and typical microglial activation are important mechanisms of NDs, leading to neurological dysfunction and disease progression. Pyroptosis is a new mode involved in this process. As a form of programmed cell death, pyroptosis is characterized by the expansion of cells until the cell membrane bursts, resulting in the release of cell contents that activates a strong inflammatory response that promotes NDs by accelerating neuronal dysfunction and abnormal microglial activation. In this case, abnormally activated microglia release various pro-inflammatory factors, leading to the occurrence of neuroinflammation and exacerbating both microglial and neuronal pyroptosis, thus forming a vicious cycle. The recognition of the association between pyroptosis and microglia activation, as well as neuroinflammation, is of significant importance in understanding the pathogenesis of NDs and providing new targets and strategies for their prevention and treatment.

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“…An increasing number of studies have revealed that secondary injury after cerebral hemorrhage can lead to a large amount of neuronal loss, and neuroinflammation plays a key role in this process [5,6]. Thus, inhibiting neuroinflammation has become an attractive possibility as an effective means to improve the prognosis of cerebral hemorrhage [7].…”

Section: Introductionmentioning

confidence: 99%

Ursolic Acid Alleviates Neuroinflammation after Intracerebral Hemorrhage by Mediating Microglial Pyroptosis via the NF-κB/NLRP3/GSDMD Pathway

Lei,

Li,

Hua

et al. 2023

IJMS

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The neuroinflammatory response after intracerebral hemorrhage (ICH) causes a large amount of neuronal loss, and inhibiting the inflammatory response can improve the prognosis. In previous laboratory studies and clinical trials, ursolic acid (UA) inhibited the inflammatory response, but whether it can be administered to inhibit the neuroinflammatory response after cerebral hemorrhage is unknown. The aim of this study was to investigate the effects of ursolic acid after cerebral hemorrhage. Online databases were used to obtain potential therapeutic targets of ursolic acid for the treatment of cerebral hemorrhage, and possible mechanisms were analyzed by KEGG, GO, and molecular docking. A rat model of cerebral hemorrhage was established using collagenase, and an in vitro cerebral hemorrhage model was constructed by adding hemin to BV2 cell culture medium. Enzyme-linked immunosorbent assay (ELISA), Western blotting (WB), immunofluorescence, TUNEL staining, and calcein/PI staining were used to investigate the degree of microglial M1 polarization, changes in the levels of inflammatory factors, activation of the NF-κB pathway, and changes in the indicators of cellular death after ursolic acid treatment. In addition, phorbol 12-myristate 13-acetate (PMA) was used to activate the NF-κB pathway to verify that ursolic acid exerts its anti-neuroinflammatory effects by regulating the NF-κB/NLRP3/GSDMD pathway. Network pharmacology and bioinformatics analyses revealed that ursolic acid may exert its therapeutic effects on cerebral hemorrhage through multiple pathways. Together, in vivo and in vitro experiments showed that ursolic acid inhibited microglial M1 polarization and significantly reduced the levels of p-NF-κB, GSDMD-N, cleaved caspase-1, TNF-α, IL-6, and IL-1β, which were significantly inhibited by the use of PMA. Ursolic acid inhibits microglial pyroptosis via the NF-κB/NLRP3/GSDMD pathway to alleviate neuroinflammatory responses after cerebral hemorrhage.

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Inhibition of Dectin-1 Alleviates Neuroinflammatory Injury by Attenuating NLRP3 Inflammasome-Mediated Pyroptosis After Intracerebral Hemorrhage in Mice: Preliminary Study Results

Cited by 13 publications

References 48 publications

Pyroptotic cell death: an emerging therapeutic opportunity for radiotherapy

Pyroptotic cell death: an emerging therapeutic opportunity for radiotherapy

To re-examine the intersection of microglial activation and neuroinflammation in neurodegenerative diseases from the perspective of pyroptosis

Ursolic Acid Alleviates Neuroinflammation after Intracerebral Hemorrhage by Mediating Microglial Pyroptosis via the NF-κB/NLRP3/GSDMD Pathway

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